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Probiotic bacteria Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG protect intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli K88

Published online by Cambridge University Press:  08 March 2007

Marianna Roselli
Affiliation:
Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN)Via Ardeatina 54600178 RomeItaly
Alberto Finamore
Affiliation:
Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN)Via Ardeatina 54600178 RomeItaly
Maria Serena Britti
Affiliation:
Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN)Via Ardeatina 54600178 RomeItaly
Elena Mengheri*
Affiliation:
Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN)Via Ardeatina 54600178 RomeItaly
*
*Corresponding author: Dr E. Mengheri, fax +39 06 51494550, email mengheri@inran.it
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Abstract

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Probiotic bacteria may provide protection against intestinal damage induced by pathogens, but the underlying mechanisms are still largely unknown. We investigated whether Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG (LGG) protected intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli (ETEC) K88, by inhibiting pathogen attachment to the cells, which is the first step of ETEC pathogenicity, and regulating neutrophil recruitment, a crucial component of inflammation. A partial reduction of ETEC adhesion was exerted by probiotics and their culture supernatant fractions either undigested or digested with proteases. ETEC viability was unaffected by the presence of B. animalis, LGG or their supernatant fractions in the culture medium, indicating an absence of probiotic bactericidal activity. Probiotics and their supernatant fractions, either undigested or digested with proteases, strongly inhibited the neutrophil transmigration caused by ETEC. Both B. animalis and LGG counteracted the pathogen-induced up regulation of IL-8, growth-related oncogene-α and epithelial neutrophil-activating peptide-78 gene expression, which are chemokines essential for neutrophil migration. Moreover, the probiotics prevented the ETEC-induced increased expression of IL-1β and TNF-α and decrease of transforming growth factor-α, which are regulators ofchemokine expression. These results indicate that B. animalisMB5 and LGG protect intestinal cells from the inflammation-associated response caused by ETEC K88 by partly reducing pathogen adhesion and by counteracting neutrophil migration, probably through the regulation of chemokine and cytokine expression.

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Type
Research Article
Copyright
Copyright © The Nutrition Society 2006